Embossed audio tag activated by touch

This disclosure describes techniques to affix an embossed pattern on an object such that when the pattern is scratched over by a hard object such a coin, pencil, or fingernail, a distinctive sonic signature is emitted. The sonic signature can be used, e.g., by a virtual assistant application, a smart speaker, or other device, to identify the object

Identification of Retinoic Acid in a High Content Screen for Agents that Overcome the Anti-Myogenic Effect of TGF-Beta-1

Transforming growth factor beta 1 (TGF-β1) is an inhibitor of muscle cell differentiation that is associated with fibrosis, poor regeneration and poor function in some diseases of muscle. When neutralizing antibodies to TGF-β1 or the angiotensin II inhibitor losartan were used to reduce TGF-β1 signaling, muscle morphology and function were restored in mouse models of Marfan Syndrome and muscular dystrophy. The goal of our studies was to identify additional agents that overcome the anti-myogenic effect of TGF-β1.A high-content cell-based assay was developed in a 96-well plate format that detects the expression of myosin heavy chain (MHC) in C2C12 cells. The assay was used to quantify the dose-dependent responses of C2C12 cell differentiation to TGF-β1 and to the TGF-β1 Type 1 receptor kinase inhibitor, SB431542. Thirteen agents previously described as promoting C2C12 differentiation in the absence of TGF-β1 were screened in the presence of TGF-β1. Only all-trans retinoic acid and 9-cis retinoic acid allowed a maximal level of C2C12 cell differentiation in the presence of TGF-β1; the angiotensin-converting enzyme inhibitor captopril and 10 nM estrogen provided partial rescue. Vitamin D was a potent inhibitor of retinoic acid-induced myogenesis in the presence of TGF-β1. TGF-β1 inhibits myoblast differentiation through activation of Smad3; however, retinoic acid did not inhibit TGF-β1-induced activation of a Smad3-dependent reporter gene in C2C12 cells.Retinoic acid alleviated the anti-myogenic effect of TGF-β1 by a Smad3-independent mechanism. With regard to the goal of improving muscle regeneration and function in individuals with muscle disease, the identification of retinoic acid is intriguing in that some retinoids are already approved for human therapy. However, retinoids also have well-described adverse effects. The quantitative, high-content assay will be useful to screen for less-toxic retinoids or combinations of agents that promote myoblast differentiation in the presence of TGF-β1

Le féminisme sur Internet : quand Internet transforme le féminisme

Ce mémoire aborde le thème du féminisme sur Internet et comme ce dernier le transforme et le façonne. Il traite avant tout des blogs, tumblrs et autres prises de paroles individuelles féministes. Dans une première partie est traitée la variété des approches féministes, qui constituent un kaléidoscope de féminismes. Dans une seconde partie, c’est l’angle du témoignage qui est abordé : pourquoi témoigner ? En quoi les sites de témoignages et les témoignages eux-mêmes sont des actes de résistance féministes ? Enfin, dans une troisième partie, le public féministe est étudié : qui est-il et que fait-il, en quoi existe-t-il un ethos féministe sur Internet ? Ce travail se termine par des recommandations à l’intention des associations féministes, et en particulier Osez le féminisme

Le féminisme sur Internet : quand Internet transforme le féminisme

Ce mémoire aborde le thème du féminisme sur Internet et comme ce dernier le transforme et le façonne. Il traite avant tout des blogs, tumblrs et autres prises de paroles individuelles féministes. Dans une première partie est traitée la variété des approches féministes, qui constituent un kaléidoscope de féminismes. Dans une seconde partie, c’est l’angle du témoignage qui est abordé : pourquoi témoigner ? En quoi les sites de témoignages et les témoignages eux-mêmes sont des actes de résistance féministes ? Enfin, dans une troisième partie, le public féministe est étudié : qui est-il et que fait-il, en quoi existe-t-il un ethos féministe sur Internet ? Ce travail se termine par des recommandations à l’intention des associations féministes, et en particulier Osez le féminisme

Characterization and expression of the rat heart sarcoplasmic reticulum Ca2+-ATPase mRNA

Sarcoplasmic reticulum Ca2+-ATPase cDNA clones have been isolated from an adult rat heart cDNA library and the nucleotide sequence of the Ca2+-ATPase mRNA determined. The sequence has an open reading frame of 997 codons. It is identical to a cDNA isolated from a rat stomach cDNA library and 90% isologous to the rabbit and human slow/ cardiac cDNAs. Nuclease S1 mapping analysis indicates that this sequence corresponds to the main Ca2+-ATPase mRNA present in heart and in slow skeletal muscle and that it is expressed in various proportions in smooth and non-muscle tissues, together with another isoform which differs from the cardiac form in the sequence of its 3′-end. © 1989.link_to_subscribed_fulltex

Regulation of myosin heavy chain and actin isogenes expression during cardiac growth

The cardiac ventricular myosin heavy chain phenotype is developmentally and hormonally regulated, but less is known concerning the actin phenotype. In this study, the levels of accumulation of α-skeletal and α-cardiac actin mRNAs were investigated in rat and human ventricles by primer extension assays. In rat, the two iso-mRNAs are present in approximately equal amounts from birth until 15 days of age and the cardiac form is predominant in adult and senescent hearts. Hypothyroid development has no effect, at least during the first two weeks of age. In man, the two isoactins are co-expressed to similar ratios in one control heart and in one failing heart. It therefore appears that myosin heavy chain and actin multigene families are both expressed in a species specific fashion but are independently regulated within a species. Preliminary results from nuclear run-on assays are presented that indicate differences in the level of transcription of the α-actin and β-myosin heavy chain isogenes in the rat heart.link_to_subscribed_fulltex

Switches in cardiac muscle gene expression as a result of pressure and volume overload

In the mammalian heart, the expression of genes encoding proteins responsible for contraction, relaxation, and endocrine function changes in hypertrophy resulting from hemodynamic overload. Different mechanisms are involved in this mechanogenic transduction, including 1) differential expression of myosin and actin multigene families, which may account for the decreased velocity of contractile element shortening in hypertrophied heart, 2) nonactivation of the sarcoplasmic reticulum Ca2+-ATPase gene, which may explain the increased duration of isometric relaxation, and finally 3) activation in the ventricle of the atrial natriuretic factor gene that is responsible in part for the high plasma levels of this peptide. It is increasingly apparent that these changes are independently regulated, but little is known about the mechanisms underlying this regulation. Preliminary results indicate that it is now possible to analyze the early time course or transcription for each gene after the imposition of hemodynamic overload. This should significantly enhance our understanding of the regulatory mechanisms involved in the phenoconversions of the hemodynamically overloaded heart.link_to_subscribed_fulltex